esults using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines (PRISMA). BACKGROUND Dioxins are persistent organic pollutants generated from industrial combustion processes such as waste incineration. To date, results from epidemiologic studies of dioxin exposure and breast cancer risk have been mixed. OBJECTIVES To prospectively examine the association between ambient dioxin exposure using a nationwide spatial database of industrial dioxin-emitting facilities and invasive breast cancer risk in the Nurses' Health Study II (NHSII). METHODS NHSII includes female registered nurses in the US who have completed self-administered biennial questionnaires since 1989. Incident invasive breast cancer diagnoses were self-reported and confirmed by medical record review. Dioxin exposure was estimated based on residential proximity, duration of residence, and emissions from facilities located within 3, 5, and 10&nbsp;km around geocoded residential addresses updated throughout follow-up. Cox regression models adjusted for breast cancer risk factors were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS From 1989 to 2013, 3840 invasive breast cancer cases occurred among 112,397 participants. There was no association between residential proximity to any dioxin facilities (all facilities combined) and breast cancer risk overall. However, women who resided within 10&nbsp;km of any municipal solid waste incinerator (MSWI) compared to none had increased breast cancer risk (adjusted HR&nbsp;=&nbsp;1.15, 95% CI 1.03, 1.28), with stronger associations noted for women who lived within 5&nbsp;km (adjusted HR&nbsp;=&nbsp;1.25, 95% CI 1.04, 1.52). Positive associations were also observed for longer duration of residence and higher dioxin emissions from MSWIs within 3, 5, and 10&nbsp;km. There were no clear differences in patterns of association for ER&nbsp;+&nbsp;vs. ER-breast cancer or by menopausal status. DISCUSSION Results from this study support positive associations between dioxin exposure from MSWIs and invasive breast cancer risk. The mechanisms and signalling pathways of the neuroprotective effect of hypercapnia and its combination with hypoxia are poorly understood. The study aims to test the hypothesis about the potentiating effect of hypercapnia on hypoxia adaptation systems directly related to hypoxia-induced factor 1α (HIF-1α). In this study we assessed HIF-1α content in hippocampal extracts and astrocytes obtained from Wistar male rats exposed to different respiratory conditions (7- or 15-fold of hypoxia and/or hypercapnia). In addition, HIF-1α content in astrocytes was assessed in in vitro model of chemical hypoxia as well as in the cerebral cortex after photothrombotic damage of this brain region. This study indicates increased levels of HIF1α in hippocampal extracts, astrocytes, and in cells of the near-stroke region of the cerebral cortex in rats exposed to hypoxia and hypercapnic hypoxia, but not hypercapnia alone. In in vitro study, hypercapnia facilitates the effects of acute chemical hypoxia observed in astrocytes. Thus, hypercapnia does not increase the level of transcription factor HIF-1α. However, the combined effects of hypercapnia and hypoxia in in vitro simulations of acute chemical hypoxia potentiate the accumulation of HIF-1α. The finite element (FE) method can potentially help in reconstructing skull fracture biomechanisms, enabling differentiation of the injury patterns caused by traffic accidents. This study aims to (1) reconstruct a motorcycle driver-car accident case using the total human model for safety and FE simulations; and (2) analyze the biomechanisms of fatal ring fractures in the motorcyclist's skull base to determine if the fatal craniocerebral injuries were caused by a fall onto the highway after hitting a pedestrian or by the subsequent impact of a car. We simulated a series of loading scenarios of falls onto the road and impacts by a car, with and without a helmet being used. We reconstructed the injury processes and compared the biomechanics results to the skull tolerance limit. For the scenario of falling with a helmet, the Von-Mises stress around the foramen magnum indicated ring fractures with a slight fracture at the impact site, consistent with that detected in a traditional forensic pathology autopsy. Moreover, we found that a helmet can significantly protect the skull by controlling the increase in stress around the impact site. However, it has very little effect on the skull base, neck, or cervical spine. We determined that the characteristic ring fracture was most probably caused by the fall onto the highway. Thus, the subsequent car accident did not contribute to the motorcyclist's death. Our study demonstrates that the FE model and method can explore injury biomechanisms, assisting in the identification of injury patterns in forensic practices. Small children put various objects into their mouths, which is one of their ways of exploring the surrounding world. Apart from toy parts, e.g. Lego® bricks or magnetic spheres, such objects include coins, small stones, as well as batteries used for different electric devices. Such batteries, especially the flat, round button type, may be ingested and become impacted in one of the physiological narrowing sites of the oesophagus, leading to serious complications. https://www.selleckchem.com/products/lee011.html The case of a 15-month-old child is presented, who died due to a massive gastrointestinal haemorrhage from an aortoesophageal fistula that developed at the site of a pressure ulcer caused by an impacted button battery. The presented case shows that ingestion of even a small battery may lead to death. The asymptomatic course of the battery ingestion significantly hinders both the assessment of circumstances and the time of the battery ingestion. Sudden death may result from a massive haemorrhage from a pressure-induced injury to a big blood vessel. Pharmaceuticals residue was detected in the water bodies as a consequence of the incomplete treatment. Recently, the side impacts of that residue on aquatic creatures have received a considerable attention. However, there is insufficient information about the effect of the most consumed narcotic drug (tramadol) on fish as an aquatic model. Thus, this study aims at investigating the poikilocytosis and tissue damage in Oreochromis niloticus after the exposure to 100 and 200 mg/L of tramadol hydrochloride. Three groups of fish were used; one as a control group, and the other two groups were exposed to 100 mg/L and 200 mg/L of tramadol hydrochloride respectively for 25 days. Exposure to tramadol caused a significant increase in the percentage of poikilocytosis compared to the control group. Poikilocytosis included tear-drop cell, spindle-shaped cell, sickle cell, schistocyte, blebbed cell, acanthocyte, eccentric nucleus, amoebocyte, dividing cell, and crenated cell. Moreover, liver tissue in fish exposed to tramadol showed degeneration and vacuolization of hepatocytes and atrophy of pancreatic acini as signs of histopathological alterations.